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Oral shedding of herpesviruses and clinical outcomes in hematopoietic stem cell transplant patients

Objectives To characterize the oral shedding of herpes viruses in patients who underwent allogeneic hematopoietic stem cell transplantation (alloHSCT) and investigate its relationship with clinical outcomes. Materials and Methods Polymerase chain reaction and enzymatic digestion were performed to id...

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Published in:Oral diseases 2023-03, Vol.29 (2), p.815-826
Main Authors: Miranda‐Silva, Wanessa, de Molla, Vinícius Campos, Knebel, Franciele Hinterholz, Tozetto‐Mendoza, Tania Regina, Arrais‐Rodrigues, Celso, Camargo, Anamaria Aranha, Braz‐Silva, Paulo Henrique, Fregnani, Eduardo Rodrigues
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Language:English
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Summary:Objectives To characterize the oral shedding of herpes viruses in patients who underwent allogeneic hematopoietic stem cell transplantation (alloHSCT) and investigate its relationship with clinical outcomes. Materials and Methods Polymerase chain reaction and enzymatic digestion were performed to identify the oral shedding of the members of the Herpesviridae family in 31 patients. The samples were collected from the oral cavity at five timestamps. Results The presence of each herpesvirus in the oral cavity was observed in 3.2%, 12.9%, 19.3%, 32.2%, 54.8% and 93.5% patients for human herpesvirus (HHV)‐6A, herpes simplex virus‐1, HHV‐6B, cytomegalovirus (CMV), Epstein–Barr virus (EBV) and HHV‐7, respectively. Oral shedding of herpes virus was not uncommon after alloHSCT. There was a statistically significant association between the EBV and CMV oral shedding at C1 and the cumulative incidence of acute graft‐versus‐host disease (aGVHD). The results suggested that the presence of HSV‐1 at C2 was related to a relapse. The HHV‐7 oral shedding at C2 suggests a possible link between relapse, progression‐free survival and overall survival of the patients. Conclusions Patients who developed aGVHD showed higher CMV and EBV shedding in the oral cavity at aplasia, suggesting modifications to the pattern of immune cell response and inflammatory microenvironment.
ISSN:1354-523X
1601-0825
DOI:10.1111/odi.14022